My lab utilizes a combined approach of molecular genetics, pharmacology, biochemistry, cell and developmental biology to understand the role of gene-environment interactions between metal exposure and neurological disease such as Huntington's disease (HD), Parkinson's disease (PD), neurodevelopmental toxicity and restless legs syndrome. We employ a diverse range of model systems including patient-derived induced pluripotent stem cells (iPSCs), neuronal cultures and mouse models. We aim to define mechanisms of neuronal dysfunction and understand the basis of selective neuropathology, by characterizing the molecular function of disease genes and their interaction with environmental toxicants under both normal and pathological conditions. My lab has established protocols to generate iPSC lines and differentiate them down cortical, striatal and midbrain neural lineages. We have developed techniques to examine toxicological and neurodegenerative/neurological related phenotypes in this patient-specific model system. In addition, we have utilized a novel high-throughput screening method to find small molecule modifiers of cellular manganese status. Recently, our work has implicated specific cellular signaling systems (e.g. p53, AKT, mTOR pathways) underlying the influence of manganese on energetics and cellular metabolism in the context of the neurological diseases we study. My labs long-term goals are to determine patient-specific and disease-specific toxicant vulnerabilities, understand the cellular pathways underlying these gene-environment interactions and develop neuroprotective strategies to mitigate neurological diseases with environmental etiologies.